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Archival Report| Volume 72, ISSUE 3, P207-214, August 01, 2012

Cortical Thickness and Folding Deficits in Conduct-Disordered Adolescents

  • Christopher J. Hyatt
    Affiliations
    Olin Neuropsychiatry Research Center, Institute of Living at Hartford Hospital, Hartford, Connecticut
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  • Emily Haney-Caron
    Affiliations
    Olin Neuropsychiatry Research Center, Institute of Living at Hartford Hospital, Hartford, Connecticut
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  • Michael C. Stevens
    Correspondence
    Address correspondence to Michael C. Stevens, Ph.D., Olin Neuropsychiatry Research Center, Hartford Hospital/The Institute of Living, 200 Retreat Avenue, Whitehall Building, Hartford, CT 06106
    Affiliations
    Olin Neuropsychiatry Research Center, Institute of Living at Hartford Hospital, Hartford, Connecticut

    Department of Psychiatry, Yale University School of Medicine, New Haven, Connecticut
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      Background

      Studies of pediatric conduct disorder (CD) have described frontal and temporal lobe structural abnormalities that parallel findings in antisocial adults. The purpose of this study was to examine previously unexplored cortical thickness and folding as markers for brain abnormalities in “pure CD”–diagnosed adolescents. On the basis of current frontotemporal theories, we hypothesized that CD youth would have thinner cortex or less cortical folding in temporal and frontal lobes than control subjects.

      Methods

      We obtained T1-weighted brain structure images from 24 control and 19 CD participants aged 12 to 18 years, matched by gender and age. We measured group differences in cortical thickness and local gyrification index (regional cortical folding measure) using surface-based morphometry with clusterwise correction for multiple comparisons.

      Results

      The CD participants, compared with control subjects, showed both reduced cortical thickness and folding. Thinner cortex was located primarily in posterior brain regions, including left superior temporal and parietal lobes, temporoparietal junction and paracentral lobule, right superior temporal and parietal lobes, temporoparietal junction, and precuneus. Folding deficits were located mainly in anterior brain regions and included left insula, ventro- and dorsomedial prefrontal, anterior cingulate and orbitofrontal cortices, temporal lobe, right superior frontal and parietal lobes, and paracentral lobule.

      Conclusions

      Our findings generally agree with previous CD volumetric studies but here show the unique contributions of cortical thickness and folding to gray matter reductions in pure CD in different brain regions.

      Key Words

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